Clearance and micropuncture studies were performed to investigate the mechanism of functional adaptation in phosphate transport in the remnant kidney of the dog in relation to the changes in sodium transport. The remnant kidney was induced by 3/4 - 5/6 ligation of the branches of renal artery which was followed by contralateral nephrectomy in 4 - 8 weeks. Five to 10 days after the nephrectomy the animals developed mild azotemia with the glomerular filtration rate reduced to about 20% of the normal two kidneys. Following extracellular volume expansion to 10% of body weight, fractional excretion of sodium increased markedly from 1.7 to 15.8% whereas the already elevated fractional phosphate excretion at 47.6% increased only minimally to 52.3%. Micropuncture of the late proximal tubule showed a significant inhibition of sodium reabsorption but unchanged values for the already high tubule fluid-to-plasma ultrafilterable phosphate ratio. A markedly elevated single nephron filtration rate was also observed. It was concluded that volume expansion has relatively little additional effect on phosphate transport in the remnant kidney when this is already inhibited maximally by phosphate adaptation. Studies were also carried out in phosphate-depleted dogs with intact kidneys placed on low phosphate diet and aluminum hydroxide gel. In early stage of phosphate depletion, phosphaturic response to volume expansion was blunted in the intact and abolished in the thyroparathyroidectomized dogs. Significant proximal tubule effect on phosphate transport was seen in both groups. In the later stage of phosphate depletion the animals responded neither to volume expansion nor to parathyroid hormone even with intact parathyroid glands. Since these changes were not related to the plasma phosphate concentration, it was postulated that intracellular phosphate concentration plays an important role in regulating renal phosphate transport. BIBLIOGRAPHIC REFERENCE: S. F. Wen: Phosphate transport in the phosphate-depleted dogs. Abstracts, 8th Annual meeting, Am. Soc. Nephrol. 1975, p.9. The paper was presented on November 26, 1975 in Washington, D.C.